Fungal infections are a significant cause of morbidity and mortality in severely ill patients, and their impact is exacerbated by a failure to rapidly diagnose and effectively treat these infections. The widespread use of antifungal agents has resulted in selection of naturally resistant fungal species, as well as the emergence of resistance in susceptible species. Treatment of fungal disease is hampered by the availability of few classes of antifungal drugs. Recently, caspofungin was introduced clinically as the first of a new class of echinocandin drugs that target the fungal cell wall by blocking β-(1→3)-D-glucan synthase. Caspofungin use is growing rapidly, and clinical isolates of Candida species with reduced in vitro susceptibility are being reported with a strong correlation between treatment failure and high in vitro values of minimum inhibitory concentration, or MIC. As patient exposure to caspofungin increases, and as the other echinocandin drugs, including micafungin and anidulafungin, enter the market, it is anticipated that the number of clinical isolates with elevated MIC values will rise.
An aspect of this invention is nucleic-acid assays that detect genetic mutations associated with resistance to echinocandin-drugs in fungi, including but not limited to fungi of the genus Candida. 
Another aspect of this invention is such nucleic-acid assays that employ exponential nucleic acid amplification of specified regions encoding the FKS1 protein, coupled preferably either with sequencing or detection utilizing labeled allele-discriminating probes.
Another aspect of this invention is kits of reagents and oligonucleotide sets of primers and probes for performing the foregoing assays.